"Our study shows an increase in the number of extrasynaptic NMDA receptors, shifting the balance between these opposing cellular mechanisms in animal models of early stages of Huntington's disease," Raymond says.

One possible interpretation of these results would be the existence of extrasynaptic KARs that could only be activated by glutamate spillover resulting from synchronous activation of excitatory fibres.

The mechanisms can include a depolarizing action of GABA (γ-aminobutyric acid), transient synaptic connections, extrasynaptic transmission, gap junction coupling and the presence of pacemaker-like neurons.